Ying Xu
Rutgers University-New Brunswick, NJ·Neuroscience
Brain cells in people with Alzheimer's disease (AD) show failing mitochondria, the cell's energy-producing structures, early in the disease. This failure seems to help drive the illness, but the cause is not well understood.
- Fields
Neuroscience
Pharmacology
- Topics
Alzheimer's disease
phosphodiesterase
cAMP
- Grants
- 1 known grant, through Apr 2027
What they work on
- Test whether removing PDE2A, an enzyme that breaks down the messengers cAMP and cGMP, from the forebrain protects against pathology and memory deficits, by crossing conditional knockout mice with Alzheimer's transgenic mouse models.
- Determine how PDE2A2, the form of PDE2A located in mitochondria, affects brain function and behavior in Alzheimer's disease mouse models.
- Explore how excess PDE2A disrupts mitochondrial dynamics, such as fragmentation, and the expression and assembly of electron transport chain complexes that power energy production in neurons.
More about the research
One candidate is PDE2A, an enzyme that breaks down cAMP and cGMP. These are small messenger molecules that help control many cell functions, including mitochondrial shape and energy production. PDE2A is especially abundant in the hippocampus and the frontal and temporal cortex, brain regions hit hard by AD.
Why it matters
Alzheimer's disease has few effective treatments. If faulty PDE2A signaling drives the mitochondrial damage seen in the disease, drugs that block PDE2A, especially its mitochondrial form PDE2A2, could become a new treatment approach. Such drugs could target energy failure in the brains of patients with Alzheimer's disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Kim Dore
University of California-San Diego, CA·Neuroscience
Measure PSD-95 palmitoylation, the fatty tag that anchors this scaffold protein in synapses, across brain regions differently affected by Alzheimer's in APP/PS1 model mice and postmortem human brain samples.
Balaji Krishnan
University of Texas Medical Branch at Galveston, TX·Neuroscience
Test how elevated levels and signaling of phospholipase D1 (PLD1), a lipid-cleaving enzyme, at synapses contribute to synaptic dysfunction and memory deficits in Alzheimer's disease and related dementias.
Colin Combs
University of North Dakota, ND·Neuroscience
Define oral health across age and disease stage in AppNL-G-F Alzheimer's model mice, including the oral microbiome, enamel thinning and cavities.
The school
Rutgers University-New Brunswick: 57 labs on PI Pages, $837M a year on research, 713 research doctorates a year.
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